Role of Cardiopulmonary Mechanoreceptors
in ADH Release in Normal Humans
BRENT EGAN, ROGER GREKIN, HANS IBSEN, KARL OSTERZIEL,
AND STEVO JULIUS
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SUMMARY Although animal studies have shown that cardiopulmonary receptors regulate the
release of antidiuretic hormone (ADH), human studies have produced conflicting results. Consequently, we studied 17 normal healthy men to determine the ADH response to selective unloading
(decreased stretch) of cardiopulmonary low-pressure receptors by thigh cuff inflation in the supine
position. Thigh cuff inflation of 30 to 40 mm Hg decreased the central blood volume and right atrial
pressure (cardiopulmonary receptor load), while mean arterial pressure and pulse pressure were
unchanged (arterial baroreceptor load). Thigh cuff inflation to this level did not alter plasma osmolality or cardiac output. Plasma ADH increased an average of 67% (p < 0.01) following thigh cuff
inflation compared to the preceding supine baseline. After thigh cuff deflation (n = 6), the ADH
decreased toward preinflation values. We conclude that selective unloading of the cardiopulmonary
receptors in humans increases plasma ADH levels. (Hypertension 6: 832-836, 1984)
KEY WORDS • vasopressin • cardiopulmonary receptors • hemodynamics
A
pressure receptors simultaneously. These orthostatic
stresses have reportedly caused either no change9 or
increases10 in plasma ADH. Others have noted that
upright posture increases plasma ADH after but not
before the induction of mild volume depletion." 12
Increasing the effective blood volume with water immersion has more uniformly suppressed urinary13 and
plasma14- '3 ADH in upright subjects. Although this
suppression has been attributed primarily to the increased load on low-pressure receptors, high-pressure
receptor load may have been altered since cardiac output (CO) increased and total peripheral resistance
(TPR) decreased.16 Furthermore, the state of osmotic
balance during water immersion is controversial and
may account for the ADH suppression during this maneuver.15- 17
The results of studies attempting to unload only lowpressure receptors in humans by either nonhypotensive hemorrhage18 or lower body negative pressure
(LBNP)19 M have also yielded conflicting results. Both
Goetzet al.18 and Goldsmith et al." reported no change
in plasma ADH with unloading of low-pressure receptors alone. Rogge and Moore20 reported significant
increases in plasma ADH after 30 minutes of LBNP at
30 mm Hg. Since mean blood pressure (MAP) and
pulse pressure did not change, they concluded that the
ADH increase resulted from selective unloading of
low-pressure receptors. However, invasive hemody-
BNORMALITIES in antidiuretic hormone
(ADH) levels1"3 and in blood volume distribution4 have been described in some hypertensive patients. It is conceivable that differences in
blood-volume distribution, through an effect on cardiopulmonary low-pressure receptors, influence the
plasma ADH level. This hypothesis can be seriously
entertained only if it were shown that low-pressure
(volume) receptors play a role in regulating ADH release in humans. The literature on volume control of
ADH release is filled with controversies.
Although decreases in blood volume,3 carotid sinus
pressure, 6 and cardiopulmonary low-pressure receptor
restraint7-8 all increase ADH release in dogs, the results of human studies are less clear. For example,
standing and tilting, which decrease central blood volume, right atrial pressure, and pulse pressure, unload
both arterial high-pressure and cardiopulmonary low-
From the Divisions of Hypertension and Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan
MedicaJ School, Ann Arbor, Michigan.
Supported in part by Grants HL 21893 and HL 18575 from the
National Institutes of Health and by the Clinical Research Center of
The University of Michigan Medical School.
Address for reprints: Brent Egan, M.D., Division of Hypertension, Box 48, R6669 Kresge Medical Research Building, University of Michigan Medical Center, Ann Arbor, Michigan 48109.
Received October 26, 1983; revision accepted May 23, 1984.
832
REGULATION OF ADH RELEASEJEgan et al.
namic data were not obtained. Therefore, the intensity
and selectivity of this stimulus are questionable.
In summary, the literature on the volume control of
ADH release in humans abounds with controversies.
Factors that regulate the relationship between intravascular volume and ADH release need to be better understood before the pathophysiology of some disease
states can be elucidated, including hypertension.
Therefore, we studied the ADH response to selective
unloading of low-pressure receptors induced by thigh
cuff inflation21 in normal human volunteers.
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Methods
Subjects
Seventeen healthy paid male volunteers, aged 18 to
34 years, participated in one of two invasive hemodynamic studies, after they had understood and signed an
informed consent form approved by the University's
Human Use Committee. All had normal results from
physical and laboratory examinations. They were put
on a standardized sodium diet (150 mEq/day) for 4
days and were given instruction sheets that included
sample menus for the 20 mEq/day Na + diet that was to
be used in the study. The diet was to be supplemented
to 150 mEq NaVday by the addition of salt tablets. The
sodium content of 24-hour urine samples was determined before the study began and was 142.0 ± 7.9
(SEM) mEq.
Laboratory Preparation
All studies began at 8:00 a.m. and ended by 1:00
p.m. Upon arrival at the laboratory, subjects assumed
the supine position and had electrocardiographic
(ECG) leads attached for heart rate (HR) monitoring.
Then, an 18-gauge, 2-inch Teflon catheter (Angiocath, Deseret Company, Sandy, Utah) was introduced
percutaneously into the left brachial artery. A No. 4
French Swan-Ganz catheter in Study 1 (Edwards Laboratories, Inc., Santa Ana, California) or a polyethylene catheter with an internal diameter of 0.58 mm in
Study 2 (Clay Adams, Division of Becton, Dickinson
and Company, Parsippany, New Jersey) was introduced percutaneously into the left basilic vein, advanced to the right ventricle, and withdrawn to the
right atrium. Statham strain gauges (Statham Instruments, Inc., Oxnard, California) were placed at midaxillary level in the fourth intercostal space for recording brachial artery (P23Db) and right atrial (P23BB)
pressures.
Hemodynamic Measurements
Details of the measurements in our laboratory have
been explained previously.22 In brief, the HR was determined from the ECG recording. Brachial artery and
right atrial pressures were obtained from the Statham
transducers connected to a Hewlett-Packard 4578
polygraph (Hewlett-Packard Company, Palo Alto,
California). The CO was measured by dye dilution
(Cardiogreen, Hynson, Westcott and Dunning, Inc.,
833
Baltimore, Maryland) with an Electronics for Medicine densitometer (Honeywell Corporation, Van
Nuys, California). Central blood volume was estimated by multiplying the CO by the mean transit time from
the right atrial to the brachial artery catheter. In addition to cardiopulmonary blood volume, the method
measures an arterial volume temporarily equidistant to
the brachial arterial sampling site.
Humoral Measurements
Plasma renin activity (PRA) was measured by radioimmunoassay of generated angiotensin I after a 60minute incubation period at a pH of 6.0. u All samples
for each subject were determined in a single assay run.
Plasma ADH was measured by a radioimmunoassay
technique developed by Pierce et al.24 The ADH was
extracted from plasma samples with octadecylsilane
cartridges (Sep-pack C l8 ; Waters Associated, Milford,
Massachusetts) by a modified method of LaRochelle et
al.25 Dried extracts were then reconstituted in 1 ml of
buffer for assay. Buffer was the same as described by
Skowski et al., 26 and antiserum was graciously supplied by Dr. Gary Robertson. l25I-arginine vasopressin
(New England Nuclear, Boston, Massachusetts) was
used as tracer, and synthetic arginine vasopressin (Sigma Chemical Company, St. Louis, Missouri) was used
for the standard curve. Standard curves based on USP
and WHO arginine vasopressin standards in the range
of from 0.63 to 80 pg/ml (0.25 to 32 uU) were linear
and parallel to curves obtained with the synthetic standard. After 7 days of incubation at 4° C, with tracer
added after 2 days, bound ADH was separated by
rabbit gamma globulin and PEG 6000 (J.T. Baker
Chemical Company, Philipsburg, New Jersey). Bound
and free fractions were counted with a Searle 1197
gamma counter. The lower limit of sensitivity in this
assay was 0.63 pg/ml. The intraassay and interassay
coefficients of variation were 6.8% and 10.4%, respectively.
Plasma osmolality was measured by freezing point
depression with a Microosmette osmometer (Precision
Systems Inc., Sudbury, Massachusetts).
Study 1
Eleven subjects participated in Study 1. After 30
minutes supine, baseline measurements were obtained
of HR, arterial and right atrial pressures, CO, central
blood volume, PRA, and ADH. Thigh cuffs were then
inflated to 30 mm Hg for 30 minutes, and the variables
were remeasured.
Study 2
Six subjects participated in Study 2. The measurements were taken 30 minutes after insertion of the
catheters with the subjects in the supine position. The
variables were the same as in Study 1, with the addition of plasma osmolality. After baseline measurements were obtained, thigh cuffs were inflated to 40
mm Hg for 30 minutes, and the variables were remeasured. At 45 minutes after thigh cuff deflation, a second
set of supine baseline measurements was obtained.
834
HYPERTENSION
TABLE 1. Hemodynamic Measurements After Thigh-Cuff Inflation
of 30 and 40 mm Hg Compared to the Preceding Supine Baseline in
17 Men
HR
MAP
PP
CO
CBV
RAP
ADH (a)
ADH (b)
PRA
OSM (n = 6)
Supine
Cuff
30-40
mm Hg
55.1 ±2.4
81.2±3.1
60.2±2.4
5.9±0.5
1824 ±109
3.9±0.7
1.7±0.4
1.5±0.3
0.95 ±0.17
284.7± 1.6
58.8±2.9
82.6±2.5
62.4±2.7
5.7±0.4
1656 ±70
2.8±0.5
7.5±5.1
2.5±0.6
1.47 ±0.26
285.7± 1.3
P
0.001
NS
NS
NS
0.01
0.03
0.01
0.01
0.03
NS
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HR = heart rate, bpm; MAP = mean arterial pressure, mm Hg;
PP = pulse pressure, mm Hg; CO = cardiac output, liter/min;
CBV = central blood volume, ml; RAP = right atrial pressure,
mm Hg; ADH = antidiuretic hormone, pg/ml; PRA = plasma
renin activity, ng/ml/hour; OSM = plasma osmolaliry, milhosmoles/liter. (a) includes and (b) excludes the subject whose ADH
increased to 87.5 pg/ml.
Supine
Cuff 40
Supine
FIGURE 1. Individual antidiuretic hormone (ADH) changes
in the she subjects in Study 2, which show an increase with thighcuff inflation and a decrease following thigh-cuff deflation.
*Values less than 0.63 pg/ml have been arbitrarily assigned a
value of 0.32 pg/ml for statistical and graphic purposes. **The
subject with ADH of 87.5 did not differ hemodynamicalty from
the others. Specifically, on continuous monitoring of arterial
blood pressure, there were no hypotensive episodes.
VOL 6, No 6, NOVEMBER-DECEMBER 1984
Statistical Analysis
Data are presented as means ± SEM. The p values
were obtained from Wilcoxon's rank-sum test of
paired differences from the supine baseline. Baseline
values of Group 1 (30 mm Hg inflation of the thigh
cuff) and of Group 2 (40 mm Hg inflation) were similar, and both levels of inflation induced similar
changes. Consequently, the data of these groups were
pooled to obtain hemodynamic and hormonal profiles
of a larger sample.
Results
Inflation of thigh cuffs to 30 to 40 mm Hg caused an
increase of ADH, PRA, and HR compared to the supine baseline. Central blood volume and right atrial
pressure decreased. The MAP, pulse pressure, CO,
and plasma osmolality did not change (Table 1).
Following the 40 mm Hg thigh cuff inflation period,
deflation of thigh cuffs was associated with a decrease
in ADH (Figure 1), although the level remained significantly (/? = 0.05) higher than at the initial baseline.
Discussion
In this study, unloading cardiopulmonary low-pressure receptors was associated with increases in plasma
ADH levels. The ability of thigh cuff inflation to unload low-pressure receptors was confirmed by decreases in central blood volume and right atrial pressure. The selective nature of this stimulus was
confirmed by an absence of changes in MAP and pulse
pressure. Therefore, it is unlikely that the high-pressure receptor load was significantly altered.27 The increases in plasma renin and HR in response to selective
unloading of low-pressure receptors confirm our previous findings.21-33-34
Our current results show that selective unloading of
low-pressure receptors increases ADH release in humans and are in agreement with results in animals.
Claybaugh and Share3 found that removal of as little as
2.6% of total blood volume in dogs increased plasma
vasopressin. Thames and Schmid8 reported that vagotomy (low-pressure receptor afferents) increased plasma vasopressin before and after carotid sinus denervation. These findings indicated that cardiopulmonary
receptors with vagal afferents tonically inhibit vasopressin release in dogs.
However, the results in humans are less uniform.
Human studies have focused on ADH responses to
relatively selective increases and decreases in cardiopulmonary low-pressure receptor load. Water immersion in upright subjects, which consistently suppresses
urinary13 and plasma ADH,14-15 is associated with significant increases in right atrial pressure and central
blood volume.16 Thus, low-pressure receptor load is
increased and likely contributes to the suppression of
ADH. Although arterial pressures are not substantially
altered, interpretation is complicated by major acute
changes in arterial hemodynamics,16 which are sustained,28 and possible hypoosmotemia,13-17 which
could also contribute to ADH suppression.
REGULATION OF ADH RELEASE/Egan et al.
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Nonhypotensive hemorrhage, lower body negative
pressure, and thigh-cuff inflation have been utilized by
various investigators to induce selective unloading of
cardiopulmonary low-pressure receptors. Rogge and
Moore20 observed an increase in plasma ADH after 30
minutes of LBNP at 30 mm Hg in humans. They assumed that LBNP elicited a selective unloading of lowpressure receptors, but they had no hemodynamic data
obtained invasively to support the assumption. Our
study uses another method to unload the low-pressure
receptors, namely, thigh-cuff inflation, and provides
information that confirms the stimulus selectivity.
Only those hemodynamic determinants that affect the
low-pressure receptor function were altered by thighcuff inflation.
Both Goetz et al. l8 and Goldsmith et al., l9 who studied the response of normal humans to nonhypotensive
decreases in effective blood volume, found the plasma
ADH unchanged. However, in both studies, plasma
for assay of ADH was obtained only 5 to 10 minutes
after unloading low-pressure receptors, which may
have been an inadequate time in which to detect ADH
changes. It is also possible that the stimulus in these
two studies18-19 was insufficient to induce increases in
plasma ADH, since Rogge and Moore,20 who found
increased plasma ADH after 30 minutes of LBNP at 30
mm Hg, did not find increased ADH after 30 minutes
of LBNP at 20 mm Hg. In addition, Rogge and
Moore20 and Goetz et al.18 used an ADH bioassay that
may have been insensitive to small changes in plasma
ADH.29 Nevertheless, Goldsmith et al.' 9 obtained
similarly negative results with the more sensitive radioimmunoassay.
An alternative explanation for the absence of an
ADH increase with 20 mm Hg LBNP may be inherent
to the method itself. Lower body negative pressure,
even when applied to the level of the iliac crests and
distally, causes decreases in gastric relaxation pressures30 and lowering of the diaphragm.31 Therefore,
negative pressure is applied to the abdominal cavity
above the vacuum chamber. This negative intraabdominal pressure may elicit mesenteric reflexes32 that
could oppose those induced by unloading cardiopulmonary low-pressure receptors. This may account for
the controversy surrounding ADH, PRA, and HR
responses to unloading of low-pressure receptors in
humans. 21 - 3334
Dietary salt intake may be another confounding
variable, since most human studies that have investigated baroreceptor control of ADH release have not
standardized dietary sodium intake. The baseline volume status may well influence the responsiveness of
this hormone to alterations in baroreceptor load." l2
For this reason, sodium intake in our study was standardized at 150 mEq/day.
Thigh-cuff inflation to 30 to 40 mm Hg caused the
elevation in plasma ADH, since the levels of this hormone decreased following cuff deflation. Our laboratory demonstrated previously that thigh-cuff inflation
causes a reflex release of renin.21-33-M We believe that
the increase of ADH with thigh-cuff inflation in the
835
present study also represents a reflex response to selective unloading of low-pressure receptors. Because systemic hemodynamics were unchanged, the increase in
ADH more likely reflects enhanced secretion rather
than diminished clearance. However, unloading lowpressure receptors may have decreased ADH clearance35 by reflexly reducing hepatic blood flow36 and by
increasing renal sympathetic nerve activity.37 In either
case, the plasma ADH increased as the result of a
reflex response with the afferent limb in the low-pressure receptors.
While the preceding discussion encompasses the
most credible reasons for the increase of ADH following thigh-cuff inflation, other explanations require
consideration. First, although two important determinants of arterial baroreceptor load were unchanged,
namely, MAP and pulse pressures,27 the rate of arterial
pressure changes (dp/dt) is also important.38-39 Dp/dt,
which was not measured in this study, may have
changed and contributed to ADH release. In another
study that elicited even larger decreases in right atrial
pressure than those recorded in this study, arterial dp/
dt was unchanged.40 Therefore, it is unlikely that
changes in high-pressure receptor load during thighcuff inflation contributed significantly to the increase
in ADH.
Second, since thigh-cuff inflation increased PRA,
elevation of angiotensin levels may have augmented
ADH release. In humans, angiotensin infusion significantly increases plasma ADH only at supraphysiologic
concentrations.41 Furthermore, we found no correlation between the magnitude of renin and ADH responses to thigh-cuff inflation (r = 0.02). Consequently, it is improbable that increases in angiotensin
caused the increase in plasma ADH.
Finally, an acute increase in the capillary-filtration
pressure of the lower extremity following thigh-cuff
inflation may have caused a temporary increase in
plasma osmolality, because of the different reflection
coefficients of the capillary membrane for water and
solutes.42 In our study, however, the plasma osmolality
was unchanged after 30 minutes of thigh-cuff inflation
to 40 mm Hg.
In summary, inflation of thigh cuffs in supine
healthy volunteers increased plasma ADH levels.
Thigh-cuff inflation decreased right atrial pressure and
central blood volume (cardiopulmonary low-pressure
receptor load), but this maneuver did not change the
MAP and pulse pressure (arterial high-pressure receptor load). The CO and plasma osmolality were also
unchanged. Our data indicate that selective unloading
of low-pressure receptors reflexly increases plasma
ADH in normal men.
Acknowledgments
We gratefully acknowledge the technical assistance of Richard
Rogers and David Brant; the secretarial assistance of Judith Mertens and Gail Tolles; and the statistical assistance of Rosalie
Kamnas.
836
HYPERTENSION
VOL 6, No 6, NOVEMBER-DECEMBER 1984
References
Downloaded from http://hyper.ahajournals.org/ by guest on June 18, 2017
1. Cowley AW, Cushman WC, Quillen EW. Vasopressin elevation in essential hypertension and increased responsiveness to
salt intake. Hypertension 1981;3(suppl I):I-93-I-100
2. Padfield PL, Brown JJ, Lever AF, Morton JJ, Robertson JI.
Blood pressure in acute and chronic vasopressin excess. N
Engl J Med 1981;304:1067-1070
3. ShimamotoT, Nakahashi Y, NakaoT, Tanaka S. Sakuma M,
Miyahara M. Plasma and urinary ADH levels in patients with
essential hypertension. Jpn Circ J I979;43:43—47
4. Esler M, Randall O, Bennett J, Zweifler A, Julius S, Rydelek
P. Suppression of sympathetic nervous function in low-renin
essential hypertension. Lancet I976;2:l 15-118
5. Claybaugh JR, Share L. Vasopressin, renin, and cardiovascular responses to continuous slow hemorrhage. Am J Physiol
1973;224:519-523
6. Clark BJ, Silva MRE Jr. An afferent pathway for the selective
release of vasopressin in response to carotid occlusion and
haemorrhage in the cat. J Physiol (Lond) 1967;191:529-542
7. Brennan LA, Malvin RL, Jochim KE, Roberts DE. Influence
of right and left atrial receptors on plasma concentrations of
ADH and renin. Am J Physiol 1971;221:273-278
8. Thames MD, Schmid PG. Cardiopulmonary receptors with
vagal afferents tonically inhibit ADH release in the dog. Am J
Physiol 1979;237:H299-H304
9. Share L, Claybaugh JR, Hatch FE, et al. Effects of change in
posture and of sodium depletion on plasma levels of vasopressin and renin in normal human subjects. J Clin Endocrinol
Metab 1972,35:171-174
10. DaviesR, Slater JDH, ForslingML, Payne N. The response of
arginine vasopressin and plasma renin to postural change in
normal man, with observations on syncope. Clin Sci Mol Med
1976;51:267-274
11. Baylis PH, Heath DA. Influence of presyncope and postural
change upon plasma arginine vasopressin concentration in hydrated and dehydrated man. J. Clin Endocrinol Metab 1977;
7:79-83
12. KimuraT, Minai K, Matsui K, etal. Effect of various states of
hydration on plasma ADH and renin in man. J Clin Endocnnol
Metab 1976;42:79-86
13. Epstein M, Pins DS, Miller M. Suppression of ADH during
water immersion in normal man. J Appl Physiol
1975;38:1038-1044
14. Epstein M, Preston S, Weitzman RE. Isosmotic central blood
volume expansion suppresses plasma arginine vasopressin in
normal man. J Clin Endocrinol Metab 1981;52:256-262
15. Greenleaf JE, Shvartz E, Keil LC. Hemodilution, vasopressin
suppression, and diuresis during water immersion in man.
Aviat Space Environ Med 1981 ;52:329-336
16. Arborelius M Jr. Balldin UI, Lilja B, Lundgren CEG. Hemodynamic changes in man during immersion with the head
above water. Aerospace Med 1972;43:592-598
17. Khosla SS, DuBois AB. Fluid shifts during initial phase of
immersion diuresis in man. J Appl Physiol 1979,46:703-708
18. Goetz KL, Bond GC, Smith WE. Effect of moderate hemorrhage in humans on plasma ADH and renin. Proc Soc Exp Biol
Med 1974; 145:277-280
19. Goldsmith SR. Francis GS, Cowley AW. Cohn JN. Response
of vasopressin and norepinephrine to lower body negative pressure in humans. Am J Physiol 1982;243:H970-H973
20. Rogge JD, Moore WW. Influence of lower body negative
pressure on peripheral venous ADH levels in man. J Appl
Physiol 1968;26:134-138
2 1 . Kiowski W, Julius S. Renin response to stimulation of cardiopulmonary mechanoreceptors in man. J Clin Invest 1978;
62:656-663
22. Julius S, Amery A, Whitlock LS, Conway J. Influence of age
on the hemodynamic response to exercise. Circulation
I967;36:222-23O
23. HaberET, KoemerT, PageLB, KlimanB, Purnode A. Application of a radioimmunoassay for angiotensin I to the physiologic measurement of plasma renin activity in normal healthy
subjects. J Clin Endocrinol Metab 1969;29:1349-1355
24. Pierce ET, Grekin RJ, Mouw DR. Efferent role of ADH in
CNS-induced natriuresis. Am J Physiol 1984;246:F32-F38
25. LaRochelle FT, North WG, Stern P A new extraction of
arginine vasopressin from blood: the use of octadecasilyl-silica. Pflugers Arch 1980;387:79-81
26. Skowski WR, Rosenblood AA, Fisher DA. Radioimmunoassay measurement of arginine vasopressin in serum: development and application. J Clin Endocnnol Metab 1974;38:278287
27. Angell-James JE, deBurgh-Daly M. Comparison of the reflex
vasomotor responses to separate and combined stimulation of
the carotid sinus and aortic arch baroreceptors by pulsatile and
non-pulsatile pressures in the dog. J Physiol I97O;2O9:257293
28. Begin R, Epstein M, Sackner MA, Levinson R, Dougherty R,
Duncan D. Effects of water immersion to the neck on pulmonary circulation and tissue volume in man. J Appl Physiol
1976;40:293-299
29. Forsling ML, Jones JJ, Lee J. Factors influencing the sensitivity of the rat to vasopressin. J Physiol 1968; 196:495-505
30. Zechman FW, Musgrove FS, Mains RC, Cohn JE. Respiratory
mechanics and pulmonary diffusing capacity with lower body
negative pressure. J Appl Physiol 1967:22:247-250
31. Milledge RD, Musgrave FS, Zechman FW. Radiographic
studies of the chest during changes in posture and lower body
negative pressure. Radiology 1968;90:674-678
32. Tuttle RS, McCleary M. Mesenteric baroreceptors. Am J
Physiol I975;299:1514-15I9
33. Julius S, Cottier C, Egan B, Ibsen H, Kiowski W. Cardiopulmonary mechanoreceptors and renin release in humans. Fed
Proc 1983,42.2703-2708
34. Egan B, Julius S, Cottier C, Osterziel K, Ibsen H. The role of
cardiovascular receptors on the neural regulation of renin release in normal man. Hypertension 1983;5:779—786
35. Streeten D, Moses A, Miller M. Disorders of the neurohypophysis. In: Thorn GW, Adams RD, Braunwald E, Isselbacher
KJ. Petersdorf RG, eds. Harrison's principles of internal medicine, 8th ed. New York: McGraw-Hill, 1977:490-501
36. Johnson JM, Rowell LB, Niederberger M, Eisman MM. Human splanchnic and forearm vasoconstrictor responses to reduction of right atrial pressures. Circ Res 1974;34:515-524
37. Zehr JE, Hasbargen JA, Kurz KD. Reflex suppression of renin
secretion during distension of cardiopulmonary receptors in
dogs. Circ Res l976;38:232-239
38. Arndt JO, Dorrenhaus A, Wiecken H. The aortic arch baroreceptor response to static and dynamic stretches in an isolated
aorta-depressor nerve preparation of cats in vitro. J Physiol
(Lond) 1975;252:59-78
39. Spickler JW, Kezdi P. Dynamic response characteristics of
carotid sinus baroreceptors. Am J Physiol 1967;212:472-476
40. Zoller RP, Mark AL, Abboud FM, Schmid PG, Heistad DD.
The role of low pressure baroreceptors in reflex vasoconstrictor
responses in man. J Clin Invest 1972;51:2967-2972
41. Padfield PL, Morton JJ. Effects of angiotensin II on argininevasopressin in physiological and pathological situations in
man. J Endocrinol 1977;74:251-259
42. Pappenheimer JR. Passage of molecules through capillary
walls. Physiol Rev 1953;33:387-423
Role of cardiopulmonary mechanoreceptors in ADH release in normal humans.
B Egan, R Grekin, H Ibsen, K Osterziel and S Julius
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Hypertension. 1984;6:832-836
doi: 10.1161/01.HYP.6.6.832
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
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